Location Of Damage In Skeletal Muscle After Lengthening Contractions

Abstract

Submaximal lengthening ("eccentric") contractions are used in everyday life, but high force lengthening contractions are associated with muscle damage and pain. The muscle-tendon junction (MTJ) is commonly cited as the primary area where myofiber damage occurs. PURPOSE: To study the location of myofiber damage resulting from muscle strain injury. In mammalian skeletal muscle, myofibers do not extend the length of the muscle. Thus, even if an injury extends throughout the cell, it cannot be assumed that damage observed in a cross section is similar throughout the whole muscle. We hypothesized that the most damage to the fibers after lengthening contractions occurs in the middle of the muscle. METHODS: Injury to the rat (N=10) tibialis anterior muscle (TA) was induced by lengthening contractions (described previously, 2007). High resolution (250μm in-plane @ 1mm slice thickness) multi-echo proton density/T2-weighted spin-echo MR images (TE1/TE2/TR=13/48/2000ms) were acquired on a Bruker Biospec 7T/30 Avance MR system to assess muscle damage on the day of injury (D0) and days 1 and 3 (D1; D3). TAs were harvested either on D0 to quantify the number of fibers with membrane damage (using IP injections of Evans Blue Dye [EBD]), or on day 14 to quantify the number of centrally nucleated fibers (using HE stain to visualize CNFs). CNFs are an accepted a marker of myogenesis that occurs after myofibers damage, but they do not appear immediately after injury. RESULTS: Injury was confirmed by a significant loss of torque (45 %). On D0, T2 values were elevated (60%) throughout the muscle belly, but limited to the MTJ by D1 after injury. The number of fibers with membrane damage was much higher in the middle of the muscle (30 ± 12% of fibers) than in the distal portion of the muscle (4 ± 1% of fibers). The occurrence of CNFs was much higher in the middle of the muscle (40 ± 8% of fibers) than in the distal muscle (5 ± 3% fibers). CONCLUSIONS: If treatments are delivered to muscle tissue to foster myogenesis and facilitate muscle growth, it is important to know where the damage is occurring. Our results suggest that myofiber injury occurs primarily in the middle portion of the muscle and that the consequent edema is initially widespread, but then limited to the MTJ. Thus, findings on MRI several days after injury may not necessarily reflect damage to the myofibers.